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J Visc Surg ; 159(1): 31-38, 2022 02.
Article in English | MEDLINE | ID: mdl-33303392

ABSTRACT

BACKGROUND: Obesity is an excessive increase in body fat mass and triggers chronic inflammation which causes increased fat accumulation in the visceral fat tissue. The aim of this study was to analyze serum zinc (Zn), Zn-alpha 2 glycoprotein (ZAG), peroxisome proliferator-activated receptor-γ (PPAR-γ) and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) levels in morbidly obese patients before and after laparoscopic sleeve gastrectomy (LSG) and determine the association between alteration in body mass index (BMI), the % Excess Weight Loss (% EWL) and the biochemical parameters. METHODS: Thirty healthy individuals as a control group and 30 morbidly obese patients who had undergone LSG were enrolled in this study. Routine anthropometric and laboratory biochemical parameters in venous blood samples of groups at baseline and 1 and 12 months after LSG were recorded. RESULTS: Significant weight loss was achieved at 1 and 12 months after LSG. At baseline serum ZAG and PPAR-γ levels were lower, while NF-кB levels were higher in morbidly obese patients compared with the control group. Serum ZAG and PPAR-γ levels increased while NF-кB levels decreased 1 month and 12 months after LSG. Decreased %EWL was negatively correlated with changes in NF-кB, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), fasting plasma glucose and insulin at 12 months after LSG in morbidly obese patients. However, %EWL was positively correlated with changes in ZAG. CONCLUSIONS: Obesity was associated with down-regulated serum ZAG and PPAR-γ levels while up-regulated serum NF-кB. Our findings suggest that LSG ameliorates upregulating PPAR-γ expression, thereby inhibiting NF-κB-mediated inflammation by weight loss.


Subject(s)
Insulin Resistance , Laparoscopy , Obesity, Morbid , Gastrectomy , Humans , Insulin Resistance/physiology , Obesity, Morbid/surgery , Weight Loss/physiology
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